In recent years there has been much interest in demonstrations of changes in the kinetic characteristics of hexose transport following oncogenic transformation of cells but little effort to demonstrate that these changes are of any metabolic consequence to the transformed cells. It is this latter consideration which defines the objectives of our current research: to assess quantitatively the roles of membrane transport and of intracellular metabolism as rate determinants of hexose uptake by animal cells. The strategies used for this assessment are: (1)\a direct measurement of isotopic flux from exogenous hexoses into cellular pools of glycolytic intermediates over short-time intervals; (2)\perturbation analysis, whereby the extent to which experimental manipulations of transport rate reflected in alterations of glycolytic rate is determined; (3) detritiation of [2-[unreadable]3[unreadable]H] glucose, which measures the glucokinase-phosphatase substrate cycle. The objects of study are normal rat hepatocytes versus Novikoff rat hepatoma cells and normal chick embryo fibroblasts versus sarcoma-virus transformed fibroblasts. Initial results with hepatocytes and hepatoma cells indicate that the control strength of transport on glycolysis is minor. The information generated should help define the role of the cell membrane as mediator of increased glycolysis in tumor cells--the much discussed but poorly understood "Warburg effect." Such information is prerequisite to an efficient search for the mechanism(s) of that effect and the design of antineoplastic drugs which might exploit that effect. (A)